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Reduced motor cortex GABABR function following chronic alcohol exposure
Shi-Yu Peng1, Zhe Shi2, Dong-Sheng Zhou3
1Shanghai Key Laboratory of Psychotic Disorders, Shanghai Mental Health Center, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Molecular Psychiatry
|January 12, 2021
Summary
Chronic alcohol exposure impairs cortical GABAB receptor function, reducing inhibitory currents. This dysfunction in GABAB receptor signaling may explain baclofen
Area of Science:
- Neuroscience
- Pharmacology
- Addiction Research
Background:
- Baclofen, a GABAB receptor agonist, treats alcohol use disorder (AUD) but its neural mechanisms are unclear.
- Understanding GABAB receptor (GABABR) function in AUD is crucial for developing effective treatments.
Purpose of the Study:
- Investigate cortical GABABR dynamics after chronic alcohol exposure.
- Elucidate the molecular mechanisms underlying GABABR dysfunction in AUD.
Main Methods:
- Ex vivo electrophysiological recordings in mice chronically exposed to alcohol.
- Analysis of GABAB1/2R and GIRK2 channel activity.
- Human paired-pulse transcranial magnetic stimulation (TMS) in patients with AUD.
Main Results:
- Chronic alcohol exposure reduced GABABR-mediated currents and GABAB1/2R and GIRK2 activities in the motor cortex.
- Alterations linked to dephosphorylation of GABAB2 subunit at serine 783, affecting receptor surface expression.
- Reduced cortical inhibition mediated by GABABR observed in human AUD patients.
Conclusions:
- Chronic alcohol exposure impairs cortical GABABR function.
- Dephosphorylation of GABAB2 subunit is a key mechanism in alcohol-induced GABABR dysfunction.
- Restoring GABABR signaling may be the therapeutic mechanism of baclofen in AUD.
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